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Article: Zinc finger E-box binding factor 1 plays a central role in regulating Epstein-Barr virus (EBV) latent-lytic switch and acts as a therapeutic target in EBV-associated gastric cancer

TitleZinc finger E-box binding factor 1 plays a central role in regulating Epstein-Barr virus (EBV) latent-lytic switch and acts as a therapeutic target in EBV-associated gastric cancer
Authors
Keywordsgene modulation
latent-lytic switch
zinc finger E-box binding factor 1
gastric cancer
Epstein-Barr virus
Issue Date2012
Citation
Cancer, 2012, v. 118, n. 4, p. 924-936 How to Cite?
AbstractBackground: The role of Epstein-Barr virus (EBV) infection in gastric carcinogenesis remains largely unknown. The authors studied the effects of zinc finger E-box binding factor 1 (ZEB1) on latent-lytic switch of EBV infection in gastric cancer and explored the importance of EBV in gastric carcinogenesis. Methods: Loss or gain of ZEB1 function was obtained by ZEB1 small-interfering RNA (siRNA) knock-down or forced ZEB1 re-expression. Cell growth was evaluated by cell viability and colony formation assays, and the cell cycle was assessed by flow cytometry. EBV was detected using quantitative polymerase chain reaction (PCR) and in situ hybridization analyses. Results: ZEB1 knock-down in a latent EBV-infected gastric cancer cell line (YCC10) increased lytic gene BamHI W leftward reading frame 1 (BZLF1) expression and decreased the expression of latent gene EB nuclear antigen 1 (EBNA1) concomitant with the inhibition of cell viability (P <.05) and S-phase DNA synthesis (P <.01). ZEB1 depletion combined with ganciclovir revealed a further reduction in cell viability (P <.001). ZEB1 knock-down induced cell apoptosis and the up-regulation of caspase 3 and poly(adenosine diphosphate-ribose) polymerase cleavage. Conversely, ectopic overexpression of ZEB1 in a lytic EBV-infected gastric cancer cell line (AGS-EBV) inhibited BZLF1 promoter (Zp) activity, BZLF1 expression, and apoptosis and promoted cell growth. EBV infection was detected in 11.3% (80 of 711) of gastric cancers. The presence of EBV was associated with age, men, and intestinal type cancer. Conclusions: ZEB1 was confirmed as a key mediator of the latent-lytic switch of EBV-associated gastric cancer, a distinct subtype with different clinicopathologic features. The current results indicated that inhibition of ZEB1 may be a potential target for EBV-associated gastric cancer therapy. © 2011 American Cancer Society.
Persistent Identifierhttp://hdl.handle.net/10722/207029
ISSN
2015 Impact Factor: 5.649
2015 SCImago Journal Rankings: 3.188

 

DC FieldValueLanguage
dc.contributor.authorZhao, Junhong-
dc.contributor.authorJin, Hong Chuan-
dc.contributor.authorCheung, Kinfai-
dc.contributor.authorTong, Joanna-
dc.contributor.authorZhang, Sui-
dc.contributor.authorGo, Minnieyy-
dc.contributor.authorTian, Linwei-
dc.contributor.authorKang, Wei-
dc.contributor.authorLeung, Patrick P S-
dc.contributor.authorZeng, Zhirong-
dc.contributor.authorLi, Xiaoxing-
dc.contributor.authorTo, Kafai-
dc.contributor.authorSung, Joseph-
dc.contributor.authorYu, Jun-
dc.date.accessioned2014-12-09T04:31:16Z-
dc.date.available2014-12-09T04:31:16Z-
dc.date.issued2012-
dc.identifier.citationCancer, 2012, v. 118, n. 4, p. 924-936-
dc.identifier.issn0008-543X-
dc.identifier.urihttp://hdl.handle.net/10722/207029-
dc.description.abstractBackground: The role of Epstein-Barr virus (EBV) infection in gastric carcinogenesis remains largely unknown. The authors studied the effects of zinc finger E-box binding factor 1 (ZEB1) on latent-lytic switch of EBV infection in gastric cancer and explored the importance of EBV in gastric carcinogenesis. Methods: Loss or gain of ZEB1 function was obtained by ZEB1 small-interfering RNA (siRNA) knock-down or forced ZEB1 re-expression. Cell growth was evaluated by cell viability and colony formation assays, and the cell cycle was assessed by flow cytometry. EBV was detected using quantitative polymerase chain reaction (PCR) and in situ hybridization analyses. Results: ZEB1 knock-down in a latent EBV-infected gastric cancer cell line (YCC10) increased lytic gene BamHI W leftward reading frame 1 (BZLF1) expression and decreased the expression of latent gene EB nuclear antigen 1 (EBNA1) concomitant with the inhibition of cell viability (P <.05) and S-phase DNA synthesis (P <.01). ZEB1 depletion combined with ganciclovir revealed a further reduction in cell viability (P <.001). ZEB1 knock-down induced cell apoptosis and the up-regulation of caspase 3 and poly(adenosine diphosphate-ribose) polymerase cleavage. Conversely, ectopic overexpression of ZEB1 in a lytic EBV-infected gastric cancer cell line (AGS-EBV) inhibited BZLF1 promoter (Zp) activity, BZLF1 expression, and apoptosis and promoted cell growth. EBV infection was detected in 11.3% (80 of 711) of gastric cancers. The presence of EBV was associated with age, men, and intestinal type cancer. Conclusions: ZEB1 was confirmed as a key mediator of the latent-lytic switch of EBV-associated gastric cancer, a distinct subtype with different clinicopathologic features. The current results indicated that inhibition of ZEB1 may be a potential target for EBV-associated gastric cancer therapy. © 2011 American Cancer Society.-
dc.languageeng-
dc.relation.ispartofCancer-
dc.subjectgene modulation-
dc.subjectlatent-lytic switch-
dc.subjectzinc finger E-box binding factor 1-
dc.subjectgastric cancer-
dc.subjectEpstein-Barr virus-
dc.titleZinc finger E-box binding factor 1 plays a central role in regulating Epstein-Barr virus (EBV) latent-lytic switch and acts as a therapeutic target in EBV-associated gastric cancer-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/cncr.26184-
dc.identifier.pmid21717425-
dc.identifier.scopuseid_2-s2.0-84856789444-
dc.identifier.volume118-
dc.identifier.issue4-
dc.identifier.spage924-
dc.identifier.epage936-
dc.identifier.eissn1097-0142-

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